Scientific article

A role of adhesion molecules in neuroglial plasticity

Published inMolecular and cellular endocrinology, vol. 140, no. 1-2, p. 89-94
Publication date1998

Glial cells are exquisitely sensitive to changes in neuronal activity, and their capacity for structural plasticity including migration is critical for remodeling an repair of nervous tissue. Our in vitro studies suggest that isoforms of the neural cell adhesion molecule (NCAM) carrying an unconventional carbohydrate polymer, polysialic acid (PSA), are involved in these events. We have demonstrated that neurohypophyseal explants from newborn rats generate cellular outgrowth of immature astrocytes displaying the characteristics of oligodendrocyte-type 2 astrocyte (O-2A) progenitor cells previously identified in the optic nerve. Treatment of O-2A cells with the enzyme Endo N, which specifically removes PSA from the cells surface, produced a complete blockade of the dispersion of the O-2A cell population from the explant. Identical effects of Endo N were observed in migration assays using cortical O-2A cells. Neurohypophyseal O-2A cells express functional NMDA class of glutamate receptors and the pharmacological blockade of these receptors inhibit PSA-NCAM biosynthesis and dramatically diminish O-2A cell migration from neurohypophyseal explants. This suggests a potential mechanism through which neuronal activity via glutamate release may regulate PSA-NCAM expression on immature glial cells, which in turn is critical for their migration.

  • Animals
  • Astrocytes/ physiology
  • Calcium Signaling
  • Cell Line
  • Cell Movement
  • Neural Cell Adhesion Molecule L1
  • Neural Cell Adhesion Molecules/ physiology
  • Pituitary Gland, Posterior/cytology
  • Rats
  • Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors/physiology
  • Sialic Acids/physiology
Citation (ISO format)
KISS, Jozsef Zoltan. A role of adhesion molecules in neuroglial plasticity. In: Molecular and cellular endocrinology, 1998, vol. 140, n° 1-2, p. 89–94. doi: 10.1016/S0303-7207(98)00034-3
Main files (1)
ISSN of the journal0303-7207

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